Since the NK 2 receptor-selective tachykinin, neurokinin A is present in fine primary afferent neurons in addition to the NK 1 receptor-selective tachykinin, substance P, we have addressed the relative role of NK 1 and NK 2 receptors in somatosensory processing in spinal dorsal horn. Recording extracellularly from rat laminae III–V neurons whilst ionophoresing drugs nearby, the selective NK 1 receptor antagonists L 688,169, GR 82334 and [D-Pro 4,D-Trp 7,910Phe 11]substance P-(4–11) failed to influence neuronal responses to cutaneous pinch or noxious heat but often enhanced responses to innocuous brush. In contrast, the highly selective NK 2 receptor antagonist L 659,874 profoundly inhibited responses to noxious heat but not pinch or brush. Highly selective synthetic agonists for both NK 1 and NK 2 receptors ([N-acetyl-Arg 6,Sar 9,Met(O 2) 11]substance P-(6–11) and GR 64349, respectively) and also NKA showed the inverse effects on sensory responses to those brought about by their antagonists. At higher ionophoretic currents, both NK 1 and NK 2 receptor agonists increased spontaneous activity. This increased basal firing induced by GR 64349 and neurokinin A (but not that due to [N-acetyl-Arg 6,Sar 9,Met(O 2) 11]substance P-(6–11) appeared to partially pre-empt further excitatory responses to noxious heat. It is concluded that although both NK 1 and NK 2 receptors can clearly mediate excitation of dorsal horn neurons, it is not NK 1, but rather NK 2 receptors that are important as the physiological transducer of brief thermal nociceptive inputs in this model.